Gilvarg C, Jockusch H, Weissmann C
Biochim Biophys Acta. 1975 Dec 19;414(3):341-8. doi: 10.1016/0005-2787(75)90172-0.
It has been reported earlier that phage Qbeta RNA (Gilvarg, C., Bollum, F.J. and Weissmann, C. (1975) Proc. Natl. Acad. Sci. U.S. 72, 428-432) elongated at its 3' terminus with up to 100 or more AMP residues retained its full infectivity for Escherichia coli spheroplasts, and that the resulting progeny did not inherit the poly (A) appendage. We now show that while poly (A)-Qbeta RNA appears to function normally as messenger for the synthesis of virus-specific proteins it has lost its capacity to serve as template for Qbeta replicase. Template function could be restored by phosphorolysis with polynucleotide phosphorylase. Taken in conjunction, these results imply that after poly (A)-Qbeta RNA enters the spheroplast a host enzyme (perhaps polynucleotide phosphorylase) removes part or all of the adenylate residues prior to replication of the RNA.
早前已有报道称，噬菌体Qβ RNA（吉尔瓦格，C.，博勒姆，F.J.和魏斯曼，C.（1975年）《美国国家科学院院刊》72卷，第428 - 432页）在其3'末端延伸有多达100个或更多的AMP残基时，对大肠杆菌原生质球仍保持完全感染性，并且产生的子代并未继承聚（A）附属物。我们现在表明，虽然聚（A） - Qβ RNA似乎能正常作为合成病毒特异性蛋白质的信使发挥作用，但它已失去作为Qβ复制酶模板的能力。通过用多核苷酸磷酸化酶进行磷酸解作用可恢复模板功能。综合来看，这些结果意味着聚（A） - Qβ RNA进入原生质球后，一种宿主酶（可能是多核苷酸磷酸化酶）在RNA复制之前会去除部分或全部腺苷酸残基。
